发病机制
疾病
医学
阿尔茨海默病
神经科学
心理学
免疫学
病理
作者
Jin Zhao,Xiaofang Wang,Yusheng He,Pingyi Xu,Laijun Lai,Younggie Chung,Xinghua Pan
标识
DOI:10.1615/critrevimmunol.2023050145
摘要
Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with memory decline and cognitive impairment, which is related to hallmark protein aggregates, amyloid-β (Аβ) plaques and neurofibrillary tangles; the latter are accumulated with hyperphosphorylated Tau protein. Immune cells play an important role in AD pathogenesis. Although the role of T cells in AD remains controversial, studies have shown that T cell deficiency is associated with increased AD pathology. In contrast, transplantation of T cells reduces AD pathology. T cells can help B cells generate anti-Аβ antibody to neutralize the toxin of Аβ and hyperphosphorylated Tau. T cells also activate macrophages to phagocytose misfolded proteins including Аβ and Tau. Recent data have also shown that AD animals have a damaged thymic microenvironment, especially thymic epithelial cells (TECs), resulting in decreased T cell numbers, which contribute to AD pathology. Therefore, regulation of T cell regeneration, for example by rejuvenating the thymic microenvironment, has the potential to be used in the treatment of AD.
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